Upregulation of adhesion molecules and class IHLA in the myocardium of chronic chagasic cardiomyopathy and heart allograft rejection, but not in dilated cardiomyopathy

The immunohistochemical expression of adhesion molecules and class I HLA in chronic chagasic cardiomyopathy were compared with heart allograft rejecti on and dilated cardiomyopathy, to obtain new knowledge on the occurrence of autoimmunity and inflammation in the pathogenesis of chronic chagasic card iomyopathy. Semiquantitative immunohistochemistry was performed for CD8+ T cells, ICAM-1, VCAM-1, LFA-1, and class I HLA in frozen sections of myocard ial biopsies from patients presenting chronic chagasic cardiomyopathy (grou p I, n = 12), heart allograft rejection (group II, n = 9) or dilated cardio myopathy (group III, n = 9). A high mean number of CD8+ T cells/mm(2) was p resent in group T (18.26) and group II (28.60), but not in group III (0.83) . The frequency of high expression for ICAM-1 and VCAM-1 on the endothelial and interstitial cells, and for class I HLA on the cardiomyocytes was grea ter in group I (100%, 33.3%, and 83.3%, respectively) and group II(100%, 66 .7%, and 77.8%, respectively), compared to group III (66.7%, 0%, and 0%, re spectively). ICAM-1 and VCAM-1 probably participate in the development of t he lymphocytic inflammatory infiltrate present in chronic chagasic cardiomy opathy, as seen in heart allograft rejection. The overexpression of adhesio n molecules and the induction of class I HLA on the cardiomyocytes are prob ably related to the high cytokine levels at the inflammatory sites in chron ic chagasic cardiomyopathy. Although the induction of class I HLA on the ca rdiomyocytes is consistent with an autoimmune reaction, it should not be co nsidered as irrefutable evidence for autoimmunity in chronic chagasic cardi omyopathy. The differential expression of adhesion molecules and class I HL A in dilated cardiomyopathy compared to chronic chagasic cardiomyopathy sug gests differences in the pathogenesis of these cardiomyopathies. (C) 2000 b y Elsevier Science Inc.